Duloxetine (Cymbalta) blocks "reuptake" of serotonin and norepi in the synapse and the result of that is more serotonin and norepi are around the receptors for longer periods. It does not block the receptors. Normally after a synapse action, the neurotransmitters go back to the cell for a waiting period..until needed again.(reuptake). I don't recall seeing any sodium ion channel activity declared for duloxetine.
http://en.wikipedia.org/wiki/Duloxetine
Duloxetine is the only antidepressant so far with serious potential to damage the liver. It can raise blood pressure, and therefore has more serious side effects than other drugs in that family like Effexor.
Cocaine's major effects are on the dopamine system, with minor effects elsewhere. Drugs are typically not "pure" in action, and often there are spill overs to other systems. An example is the serotonin release some opiates cause (oxycodone). Cocaine has historically been chemically modified, to other drug entities like lidocaine, to remove the euphoric dopamine effects, and to leave the sodium ion channel effects and hence have totally different pharmacologic targets.
Neurotransmitter actions are very complex, and we've learned that SSRIs for example don't really do what was initially thought. More time and research are needed to understand their complex actions.
But the current belief is that duloxetine, works on the serotonergic pathways in the brain that interpret subjective pain signals. TCAs like amitriptyline and nortriptyline also work in the same way. However, new studies are showing TCA's ...specifically amitriptyline may enhance growth factors, in nerves and help with healing. The SSRI's do not have this function as yet discovered.
Quote:
Originally Posted by JoeTheToad
I'm an old dog, but I'll cope with new concepts.
I never take a medication without gaining some measure of an idea as to how they work. Reading up about duloxetine and having noticed it blocks two of the same neurotransmitters as cocaine, am wondering if its anesthetic qualities similarly stem from blocking sodium ion channels?
I must admit I enjoyed the happy feelings that came with gabapentin (at least for me), but its pain killing properties were negligible. Pregabalin is more effective, but I don't like the side effects. On gabapentin I felt sharp as a pin, whereas I feel a bit blunt on pregabalin.
My experience is that the medical profession don't have a clue about neuropathy. I'm on my third neurologist, as the first two hadn't read my notes, which was plainly obvious. The new one is better, but would be after I'd lobbed an exec complaint at the hospital (on account of the neurologist mistaking pregabalin for gabapentin, and recommending I increase dosage by a factor of three (and I was on 600mg which she said was a 'baby dose')). Just as well I don't automatically trust what they say, as an increase to 1800mg of pregabalin may have been a bit much even for my system!
Doctors seem to have a list of medications which they'll throw at you until they find one which seems to do more than the others, without such unpleasant effects as some. Other than that, they seem pretty mystified.
I'd rather speak to people who've gone through trial and error, so you'll find me open-minded!
Joe
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All truths are easy to understand once they are discovered; the point is to discover them.-- Galileo Galilei
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